Brain somatostatin receptors in a rat model of acute liver failure

The present study examines the effect of acute liver failure induced by a single intraperitoneal (i.p.) injection of D-galactosamine-HCl (3 g/kg) on somatostatin (SS) binding and levels in the rat frontoparietal cortex and hippocampus. Neurobehavioural changes were evaluated by the method of Zieve et al. [(1984) J. Lab. Clin. Med., 104:655-664]. The rats were decapitated as soon as they reached neurobehavioural stage I or II. In stage I, rats had lethargy and in stage II they showed mild ataxia, mainly in the hind limbs. The administration of D-galactosamine elevated serum transaminase levels (mean peak level 2,242 IU/1) but hypoglycemia, gross cerebral edema, or signs of sepsis were not detected in any of the animals studied. In addition, D-galactosamine did not affect somatostatin-like immunoreactivity (SSLI) levels in either brain area in any of the experimental groups as compared to the control groups. The rats sacrificed in stage I showed no change in the number or affinity of specific 125I-Tyr11-somatostatin (125I-Tyr11-SS) receptors in synaptosomes from the frontoparietal cortex and hippocampus. The rats sacrificed in stage II showed a decrease in the number of specific 125I-Tyr11-SS receptors in synaptosomes from both brain areas, with no change in receptor affinity. Binding studies were also conducted on synaptosomes from the frontoparietal cortex and hippocampus of rats that received D-galactosamine but did not develop acute liver failure and consequently did not develop neurobehavioural changes. The SS receptors in these synaptosomes did not change in comparison with controls, indicating that the D-galactosamine was not directly responsible for the changes in the cerebral SS receptors.(ABSTRACT TRUNCATED AT 250 WORDS)